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Collaborators Denis S. Grebenkov, PhD
Collaborators Denis S. Grebenkov, PhD
 Denis S. Grebenkov, PhD Personal Webpage My Laboratory Ecole Polytechnique The mature placenta is a complex arborized vascular bed extending from the umbilical arteries to the chorionic surface vessels, to the fetal stem vessels and ultimately to the capillary beds of the terminal (nutrient) villi, the anatomical sites of all oxygen and nutrient exchange between the mother and the fetus. The capillary beds drain into a venous system that parallels the arterial tree, ultimately draining into chorionic surface veins and the umbilical vein that carries blood to the fetus. The anatomical site of oxygen exchange, the vasculosyncytial membrane has been well studied as a vector of diffusive conductance. From the perspective of maternal perfusion, intervillous blood flow will access individual terminal villi at different flow rates. This is analogous to what happens in the bronchial tree of the lungs, in which fresh air is inhaled through the mouth at relatively high velocity and then substantially slowed down as it moves into the distal bronchioles (with their greater total cross-section area). At this point, several questions naturally arise: How does the geometry of the placental villous architecture determine the oxygen and carbon dioxide transport efficiency? How is the oxygen flux correlated with gestational age, birth weight and other perinatal outcomes? Various processes (maternal diseases, environmental exposures, etc.) can lead to abnormal growth of the placental villous tree. Abnormal development of the placental villous tree (over growth or sparse branching) makes either or both maternal uteroplacental blood flow around the villi and fetoplacental blood flow within the villi less efficient; both contribute to abnormal placental-fetal transport. Transport is efficient only when all the terminal villous surfaces are equally accessible to the maternal uteroplacental intervillous blood. However, an abnormally grown placenta with an increased number and/or size of villi (e.g., diabetic placentas) may have “crowded” villi. Villi in too close proximity may “shield” other villi from the maternal perfusion and limit their function. In the lung, this has been termed “screening”. As a result of overcrowding, maternal blood cannot flow easily around these terminal villi, and transfer of oxygen from the maternal circulation across the villus surface may be substantially reduced. This situation is clearly illustrated in a 2d cut of a pathological placenta in Fig. 2. Dense packing of the villi makes them more “screened” to the flow of the maternal uteroplacental intervillous blood. Conversely, too sparse villous arborization results in maternal uteroplacental intervillous blood flow that cannot adequately access terminal villi; maternal blood may flow into and out of the intervillous space without encountering villi and transferring any oxygen, another type of inefficiency. From this functional point of view, the difference between normal and pathological placentas resembles the difference in functioning of the lung acinus at exercise and at rest. In the normal placenta, all the terminal villi are accessed more or less equally around their entire perimeter by the maternal uteroplacental intervillous blood (as the alveolar membrane is accessed by oxygen at exercise, Fig. 1). In pathologically “overgrown” placentas, the intervillous space is crowded with villi so that only a fraction of the terminal villous surfaces can be accessed (only a part of the alveolar membrane near the acinus entrance is accessed at rest, Fig. 1).
Our goal is to evaluate the diffusion efficiency of normal and diseased placentas and determine whether such measures correlate with gestational age, birth weight and other perinatal outcomes. Downloads (right click and select "save target as") Denis S. Grebenkov - CV |
